Chlamydia Infection Case Study
Although chlamydial persistence in vitro was proven and characterized in many studies [27–33], it is hard to identify persistency in vivo and until recently it was unknown if it even exist in the host. However, in a recent paper characterizing genital chlamydial infections in two patients, evidence of persistence growth forms were found and isolated, and the morphological and molecular analysis showed that chlamydial persistency does exist in vivo in some patients [31]. Women that acquire new infections or are unable to fully clear their infection are more prone to diseases such as pelvic inflammatory disease (PID), endometriosis, life threatening ectopic pregnancy and infertility [36–38]. Progression to severe sequelae is thought to be the
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However, C. trachomatis is capable of evading the host innate and adaptive immune response using many different mechanisms while resides in the genital epithelial cell [42–46]. Studies using a prospective cohort of women in high risk for chlamydia infection show that efficient immune response that correlate with protection against infection or reduced risk for reinfection, consist of the production of IFN-γ by peripheral-blood mononuclear cells (PBMCs) …show more content…
The epithelial cells, which are primary targets of chlamydiae, act as the first line of defence, forming a selective barrier with intracellular tight junctions, which effectively restrict trans-epithelial movement of molecules (Wyrick, 2006). Studies have focused on the central role of epithelial cells in initiating and orchestrating the immune response after pathogen challenge at this site [50]. These multiple roles include thickening of the epithelial cell layer, production of mucins and the constitutive and induced expression of a wide range of antimicrobial mediators including the epithelial defensins, secretory leucocyte protease inhibitor (SLPI) and cathelicidins [51–53]. The detection of invading microbes occurs through the recognition of a highly conserved structure present on the outer membrane of the bacteria (Pathogen associated molecular patterns; PAMPs). The PAMPs are recognized by different families of receptors such as Toll-like receptors (TLRs) and NOD/CARD present on the epithelial cells as well as the immune cells [52,54]. Immediately after the recognition there is an activation and release of chemokines and cytokines (such as IFN-γ). These proteins elicit leukocyte migration to the infected area and further activation of additional innate effectors cells including macrophages,
However, C. trachomatis is capable of evading the host innate and adaptive immune response using many different mechanisms while resides in the genital epithelial cell [42–46]. Studies using a prospective cohort of women in high risk for chlamydia infection show that efficient immune response that correlate with protection against infection or reduced risk for reinfection, consist of the production of IFN-γ by peripheral-blood mononuclear cells (PBMCs) …show more content…
The epithelial cells, which are primary targets of chlamydiae, act as the first line of defence, forming a selective barrier with intracellular tight junctions, which effectively restrict trans-epithelial movement of molecules (Wyrick, 2006). Studies have focused on the central role of epithelial cells in initiating and orchestrating the immune response after pathogen challenge at this site [50]. These multiple roles include thickening of the epithelial cell layer, production of mucins and the constitutive and induced expression of a wide range of antimicrobial mediators including the epithelial defensins, secretory leucocyte protease inhibitor (SLPI) and cathelicidins [51–53]. The detection of invading microbes occurs through the recognition of a highly conserved structure present on the outer membrane of the bacteria (Pathogen associated molecular patterns; PAMPs). The PAMPs are recognized by different families of receptors such as Toll-like receptors (TLRs) and NOD/CARD present on the epithelial cells as well as the immune cells [52,54]. Immediately after the recognition there is an activation and release of chemokines and cytokines (such as IFN-γ). These proteins elicit leukocyte migration to the infected area and further activation of additional innate effectors cells including macrophages,